BJD

R EV IE W AR TI C LE British Journal of Dermatology

Atopic dermatitis in the elderly: a review of clinical and

pathophysiological hallmarks*
S. Williamson iD , J. Merritt and A. De Benedetto
Department of Dermatology, College of Medicine, University of Florida, Gainesville, FL, U.S.A.

Linked Comment: Szegedi. Br J Dermatol 2020; 182:9–10.

Summary

Correspondence Background Atopic dermatitis (AD) is a multifactorial and complex disease, charac-
Anna De Benedetto. terized by an impaired skin barrier function and abnormal immune response.
E-mail: adebenedetto@ufl.edu Many elderly patients present with pruritus and xerosis to dermatology, allergy
and primary care clinics, and there is a lack of information available to clinicians
Accepted for publication
15 March 2019 regarding the proper diagnosis and management of these patients. Although the
elderly are described as having a distinct presentation of AD and important
Funding sources comorbidities, most investigations and clinical care guidelines pertaining to AD
S.W. was supported by the Medical Student Sum- do not include patients aged 60 years and older as a separate group from
mer Research Program at the University of Florida,
younger adults.
College of Medicine.
Objectives To summarize current information on pathophysiology, diagnosis and
Conflicts of interest management of AD in the elderly population and identify areas of insufficient
A.D.B. served as consultant for Regeneron and information to be explored in future investigations.
Sanofi Genzyme. All authors have read the manu- Methods We carried out a systematic review of published literature, which assessed
script and have approved submission. changes in the skin barrier and immune function with ageing and current infor-
mation available for physicians to use in the diagnosis and treatment of AD in
*Plain language summary available online
elderly patients.
DOI 10.1111/bjd.17896 Results Many age-related changes overlap with key hallmarks observed in AD,
most notably a decline in skin barrier function, dysregulation of the innate
immune system, and skewing of adaptive immunity to a type-2 T helper cell
response, in addition to increased Staphylococcus aureus infection.
Conclusions While general physiological alterations with ageing overlap with key
features of AD, a research gap exists regarding specific ageing-related changes in
AD disease development. More knowledge about AD in the elderly is needed to
establish firm diagnostic and treatment methodologies.

What’s already known about this topic?

• Atopic dermatitis (AD) is a common inflammatory skin disease that causes signifi-
cant burden worldwide.
• Recently, elderly patients have been considered a subgroup of patients with distinct
AD manifestation.
• Limited studies have characterized the clinical presentation and role of IgE-
mediated allergy in elderly patients with AD.

What does this study add?

• This review offers a summary of age-related skin and immune alterations that cor-
respond to pathogenic changes noted in patients with AD.
• The role of itch, environmental factors and skin microbiota in AD disease presenta-
tion in ageing patients is explored.

© 2019 British Association of Dermatologists British Journal of Dermatology (2020) 182, pp47–54 47
48 Atopic dermatitis in the elderly, S. Williamson et al.
Atopic dermatitis (AD) is the most common chronic inflam-
matory skin condition and leading cause of disease burden
among nonlethal skin conditions.1,2 AD is characterized by
eczematous rash, diffuse xerosis, intense pruritus and recurrent
Staphylococcus aureus infection.3 Patients with AD often have
atopy, including asthma, allergic rhinitis, and environmental
and food allergies.4 The clinical manifestations of AD tend to
vary with age.5 Three groups of patients with AD have been
well established based on appearance and localization of
eczematous lesions at different ages, i.e. infantile type, child-
hood type, and adolescent and adult type.6 In infants (infantile
type), AD typically presents as acute eczematous crusting pla-
ques on the face, and scales on the scalp.5 Childhood-type AD
is characterized by acute and chronic lesions often involving
the flexural aspects of limbs and around the mouth, nose and
eyes,5 while adult-type AD tends to present with diffuse liche-
nified plaques at the flexural surfaces, head and neck.5 Elderly-
type AD has recently been considered a fourth separate group,
presenting more commonly with the reverse sign of licheni-
fied eczema at the antecubital and popliteal fossae than with
lesions localized to the creases of the folds, as is typical of
adult-type AD.5,7 Patients with elderly-type AD can be further
subdivided by disease onset, i.e. infancy or childhood onset
with recurrence or continuation of AD at age ≥ 60 years; ini-
tial onset in adolescence or adulthood with recurrence or con-
tinuation of AD at age ≥ 60 years; and primary onset of AD at
age ≥ 60 years.8
This review presents the current information available
regarding ageing-related AD pathophysiology, which is an
evolving field of knowledge, as few articles have characterized
AD in the elderly population.7,9–12
Epidemiology
More than 230 million people worldwide have a diagnosis of
AD,1 a disease with high prevalence in children (15–30%)
and adults (2–10%),6 but there is limited prevalence data for
the elderly. In Saarland, Germany, the prevalence of AD in
patients aged 60–69 years was ~4%.13 In Poland, AD preva-
lence was 2% for the elderly population (≥ 60 years),10 com-
pared with ~5% of children (6–7 years),14 ~4% of adolescents
(13–14 years)14 and ~3% of adults (20–44 years).14 Similarly,
~3% of elderly patients ≥ 60 years15 and ~4% of adults (30–
39 years)15 who visited a Tokyo hospital had AD, compared
with ~19% of children (7–9 years)16 in Otsu, Japan. A multi-
centre cross-sectional study produced in France reported a
high prevalence of xerosis in the elderly (~56% of patients
aged ≥ 65 years) and found that a history of atopy, especially
AD, is associated with significantly increased risk of xerosis in
elderly patients.17
Pathophysiology
The pathogenesis of AD is complex and multifactorial (as
described by Weidinger et al. in their comprehensive review).1
Hallmarks of the disease are an impaired skin barrier and
British Journal of Dermatology (2020) 182, pp47–54
abnormal T helper (Th)2-skewed immune response to envi-
ronmental antigens and allergens. Traditionally, the following
two hypotheses have been proposed: (i) inside out, in which a
primary immune system defect drives skin damage and der-
matitis, and (ii) outside in, in which the primary skin barrier
defect is thought to determine the aberrant immune
response.18 A growing body of evidence now suggests that in
either case, there is active crosstalk between skin barrier and
immune system; once one arm is perturbed, it can affect the
other, feeding a vicious cycle that likely supports disease
chronicity.
Bacterial colonization and recurrent skin infection are two
important factors associated with disease severity. In addition,
itch is a key feature of AD lesions. These components are neg-
atively correlated with quality of life and need to be consid-
ered essential elements in the disease pathogenesis. The
hypothesis of AD pathogenesis is developing to include age as
a subphenotype, which contributes to different mechanisms of
disease development and clinical presentation.5 Well-estab-
lished skin barrier and immune system changes associated
with ageing likely contribute to this process (summary in
Fig. 1 and Table 1).
Physical skin barrier
Ageing skin is classically associated with reduced physical bar-
rier function,19–24 which contributes to AD exacerbation in
older patients. Ageing skin is thinner, more translucent, and
undergoes elastosis, rendering it more physically fragile.19–24
Epidermal stem cells at the dermoepidermal interface regularly
replenish keratinocytes.25 As skin ages, a normal number of
these stem cells are still present, but their ability to migrate
Fig 1. The impact of ageing on factors contributing to the
pathogenesis of atopic dermatitis (AD). TEWL, transepidermal water
loss; Th2, T helper cell type 2; TJ, tight junction; TLR, Toll-like
receptor.
© 2019 British Association of Dermatologists

Table 1 Summary of ageing-related changes in skin barrier and immune system and overlap with known abnormalities in atopic dermatitis (AD)
Age-related changes
Skin barrier
Filaggrin is downregulated
Claudin-1 and occludin proteins are downregulated
Decreased barrier repair occurs
after irritation (based on increased TEWL)
Innate immunity
PRRs decline in function
Phagocytic function of PMNs decreases
Adaptive immunity
Possible Th2 shift occurs
IgE+ CD1a+ DCs and mast cells are increased in skin
TEWL, transepidermal water loss; PRR, pattern recognition receptor; cDC, conventional dendritic cell; PMN, polymorphonuclear leucocyte;
Th2, T helper cell type 2; DC, dendritic cell; FceRI, high-affinity IgE receptor; FceRII, low-affinity IgE receptor.
and respond to proliferative signals declines.26 The rate of
new keratinocyte production in the epidermis decreases with
ageing,25 and collagen fibres comprising the dermal extracel-
lular matrix become fragmented and disordered.27
The stratum corneum (SC) serves as the primary component
of the skin barrier.19 The epidermal cornified envelope com-
position differs considerably as skin ages, contributing to
decreased barrier function.28,29 The cornified envelope is com-
posed of a keratin and filaggrin protein network stabilized by
cross-linking transglutaminases and surrounded by a lipid
layer.28 With ageing, certain cornified envelope proteins are
upregulated and others (i.e. filaggrin) are downregulated.29
FLG null mutations are a major predisposing factor to AD
development,1 and while genetic mutations are likely noncon-
tributory in the pathogenesis of new-onset AD in elderly
patients, age-related decline in filaggrin production may be a
contributing factor.
Tight junctions (TJs) are cell–cell connections located under
the SC, which contribute to epidermal barrier integrity.30–32
Epithelial TJs are composed of proteins including claudin
(CLDN), occludin and zonula occludens.30,31 CLDN1 is inte-
gral to TJ functionality in the skin barrier.31,33 CLDN1 muta-
tions are associated with skin xerosis, pruritus and AD
development.31,32 Jin et al. demonstrated changes in epidermal
TJ protein constituents in older skin (from patients aged ≥ 75
years) compared with younger skin, suggesting that TJ dysreg-
ulation could play a role in AD pathogenesis in the elderly.31
Intrinsically aged skin was characterized by downregulation of
CLDN1 and occludin proteins. In the same patients, photoaged
skin sampled from the forearm displayed decreased CLDN1
expression compared with intrinsically aged skin from the
buttock.31
Transepidermal water loss (TEWL) is a well-established
method used to measure skin barrier integrity in vivo.34 While
one could speculate that the aforementioned age-related
© 2019 British Association of Dermatologists
Atopic dermatitis in the elderly, S. Williamson et al. 49
Hallmarks in AD
Filaggrin null mutations are a strong genetic risk factor for AD
Reduced expression of claudin-1, -4 and -23 noted in nonlesional AD skin
Increased TEWL occurs at baseline and after tape stripping in nonlesional skin
PRR expression and function are impaired in cDCs and skin
Phagocytic capacity of PMNs in skin declines
Th2 (+ Th17/T22) skewed immune infiltrate noted in acute lesions, with
Th1 cells also detected in chronic lesions
Increased FceRI on CD1a+ epidermal DCs and FceRI and FceRII on monocytes
detected in peripheral blood samples
deterioration of the skin barrier would consistently result in
higher TEWL, some discrepancies exist among the analyses of
the relationship between ageing and TEWL. Roskos et al. deter-
mined that there was no difference in baseline TEWL rates,
measured using the ServoMed EPIC unventilated evaporimeter
(ServoMed, Stockholm, Sweden), between individuals aged
< 43 years and > 68 years. However, after occlusion of skin
that mimicked a stressed condition, TEWL rates were higher
and returned to baseline levels more slowly in the elderly
group,35 suggesting impaired barrier recovery function. A
meta-analysis of studies measuring TEWL across age groups
reported lower TEWL in people aged over 65 years,34 which
contrasted with another study reporting similar baseline TEWL
in the elderly and younger adults.35
The ability to repair the skin barrier after irritation is dimin-
ished in elderly individuals.36 Barrier recovery after insult by
tape stripping or acetone application, determined by measur-
ing TEWL values at various time intervals after insult, was
deficient in the elderly (aged > 80 years) compared with
young (aged < 30 years) volunteers.37 Following insult, the
decreased TEWL took longer to increase to baseline levels in
older participants, demonstrating that barrier recovery is
appreciably slower in aged skin.37
Altogether, strong evidence suggests that physical or envi-
ronmental irritation, in combination with a defective aged
epidermal barrier, may contribute to AD development in the
elderly.
Immune system
The immune system becomes dysregulated with age and is
characterized by chronic inflammation – a concept referred to
as ‘inflammageing’.38,39 Inflammageing is thought to be a
consequence of a remodelling of the innate and adaptive
immune system, resulting in chronic inflammatory cytokine
British Journal of Dermatology (2020) 182, pp47–54
50 Atopic dermatitis in the elderly, S. Williamson et al.
production. Notably, some of the age-related changes in the
immune system are analogous to defects observed in patients
with AD. However, it is important to disclose that similarities
do not mean that these changes, if present, are mechanistically
involved in elderly AD pathogenesis. Specific studies are
needed to provide further confirmation of causality for the
changes in elderly AD.
Innate immunity
The innate immune system decline with age includes changes
in cell number and function in addition to changes in the
expression of pattern recognition receptors (PRRs) and their
involved signalling pathways.38 Based on studies of peripheral
blood, expression and function of Toll-like receptors (TLRs)
in dendritic cells (DCs), polymorphonuclear (PMN) leuco-
cytes, and monocytes decrease with age, causing innate
immune cells to be less capable of killing bacteria.40,41 Skin
macrophages produce less tumour necrosis factor and fewer
neutrophils are recruited, leading to impaired wound heal-
ing.38 Decreased neutrophil and eosinophil functional ability
contributes to weaker defences against bacteria and microor-
ganisms.38,42 In older people, neutrophils have impaired
pathogen-killing ability owing to declining phagocytic func-
tion such as opsonization and production of reactive oxygen
species.38
A variety of defects have been identified in the innate
immune system in AD including dysfunction in PRRs and
diminished recruitment of innate immune cells (e.g. PMNs
and plasmacytoid DCs) to the skin (De Benedetto et al.,43
McGirt and Beck44 and Wollenberg et al. have reviewed this
topic).45 Skin biopsies of patients with AD have been found to
lack PMNs, notably even with S. aureus infection or skin
scratching.44 PMNs are observed to display functional impair-
ment in AD, including defective chemotactic activity and
impaired phagocytic capacity,43,44 similar to changes with
ageing. Overall, the effectiveness of the immune system to
defend the body against pathogens declines with age,38 ren-
dering the elderly more susceptible to severe and chronic
infections.40 The irreversible decline in innate immune cell
function may contribute to the difficulty in the treatment and
cure of elderly patients with AD.
Adaptive immunity
Ageing is associated with profound change in the adaptive
immune system. As people age, naive Th0 cells become less
functional and produce less interleukin (IL)-2, while Th1 and
Th2 cells increase cytokine production.46 IL-3, IL-4 and inter-
feron (IFN)-c play an important role in cellular and humoral
immunity, but inconsistent data have been found regarding
their expression in the elderly. An increased production of IL-
5 and IL-10 has been more consistently observed, favouring a
shift towards the Th2-type immune response.47
Two cytokines produced by the Th2 inflammatory response,
namely IL-4 and IL-13, have a key role in the pathogenesis of
British Journal of Dermatology (2020) 182, pp47–54
AD.48 The presence of IL-4 and IL-13 during keratinocyte dif-
ferentiation leads to a weakened physical skin barrier resulting
from reduced production of structural epidermal protein com-
ponents including filaggrin, loricrin and involucrin.48 IL-4 and
IL-13 also prevent production of antimicrobial peptides and
downregulate Th1- and Th17-dependent immune responses in
the skin, leading to increased susceptibility to S. aureus infec-
tion.48 Another cytokine associated with Th2 inflammation,
namely IL-31, contributes to itch and has been implicated in
AD and noted to be elevated in the ageing population.49–52
Elevated levels of IL-31 and IL-31-producing T cells have been
detected in AD skin lesions.51,53 S. aureus superantigen was
shown to induce IL-31 expression and T-cell recruitment, and
mediate pruritus in patients with AD.53 AD tends to be very
itchy in elderly patients; it remains to be determined whether
this is associated with increased expression of IL-31 or its
receptors in elderly AD skin.
Patients presenting with AD at age 60 years or older
often have very high levels of IgE, which is considered a
marker of Th2 inflammation.5 While serum IgE decreases
with age in patients with allergic rhinitis and asthma, no
significant decrease is shown with age in patients with
AD.54 Elderly patients with AD can be classified into IgE-
allergic type (60–80% of patients, namely extrinsic AD) and
non-IgE allergic type (20–30% of patients, namely intrinsic
AD), according to total serum IgE and allergen-specific IgE
levels.7,10 Elderly patients with IgE-allergic AD have a Th2-
dominant cytokine profile in peripheral blood including IL-
4, IL-5 and IL-13, whereas elderly patients with non-IgE-
allergic AD are skewed towards a Th1-dominant profile
including IL-2 and IFN-c.7 Chronic lichenified lesions of
elderly patients with IgE-allergic type AD were noted to
have infiltrating IgE+ CD1a+ DCs in the epidermis, CD11c+
DCs in the epidermis and upper dermis, and IgE+ mast
cells in the upper dermis,8 while in comparison, the
chronic lesion of an elderly patient with asteatotic (nonato-
pic) dermatitis contained only CD11c+ DCs.8 This result is
similar to those of other studies performed across age
groups. IgE-allergic type AD lesions of patients not being
treated with local or systemic glucocorticoids had signifi-
cantly increased levels of high-affinity IgE receptor (FceRI)
on CD1a+ epidermal DCs compared with both normal con-
trol skin and non-IgE-allergic AD skin lesions.55 Peripheral
blood of patients with nonglucocorticoid-treated IgE-allergic
AD was shown to have monocytes with significantly higher
levels of FceRI and FceRII compared with that of nonatopic
control patients, and significantly increased levels of FceRI
compared with monocytes in the peripheral blood of
patients with non-IgE-allergic AD.56 These cell types impli-
cated in IgE-allergic type AD can lead to cutaneous hyper-
sensitivity reactions owing to the accumulation of IgE and
allergen complexes in upper skin layers.7
In summary, age-related changes in the immune system
align with defects typically observed in AD, and it remains to
be determined whether those changes are directly involved in
AD pathogenesis.
© 2019 British Association of Dermatologists

Pruritus
Pruritus has complex and varied pathomechanisms57 in AD
involving histamine- and nonhistamine-responsive afferent
sensory C-fibres that relay signals regarding cutaneous itch to
the central nervous system.58,59 Pruritus is a common and dis-
tressing symptom affecting one-quarter of patients over the
age of 65 years seen annually in U.S. outpatient clinics60 and
affects a significant proportion of patients in other regions.
Pruritus in the elderly is most often secondary to xerosis and
is commonly associated with other dermatological conditions,
including AD.57,61 Whether pruritus plays a direct role in the
pathogenesis of AD in the elderly has not yet been investi-
gated.
Skin microbiota
Patients with AD are susceptible to bacterial skin infections
owing to physical skin breakdown, dysregulated skin antimi-
crobial immunity, and bacterial colonization.62,63 Patients with
AD have less heterogeneous colonizing skin bacteria and an
increased presence of S. aureus.9,63 More severe AD flares are
associated with decreased skin bacterial diversity.64 A high
prevalence of S. aureus colonization has been noted in the
elderly population. In Swedish nursing homes, 48% of
patients aged ≥ 60 years were found to have S. aureus coloniza-
tion in the nares,65 compared with a prevalence of ~32% in
people aged 4–19 years reported throughout Sweden.66
There is a diversity that has been observed when the skin
microbiome of younger people has been compared with that
of older individuals. Older Thai men (51–57 years) were
found to have a predominance of Rhizobiales order, Sphingomonas
and Pseudoalteromonas bacteria on the cheek and forehead,
whereas the skin of young adult men (19–24 years) was
skewed towards Propionibacterium and Staphylococcus epidermidis bac-
teria.67 A study comparing Japanese women of various ages
noted increased alpha diversity in forearm, forehead and cheek
skin, and increased beta diversity of the forearm and scalp in
elderly women (60–76 years) compared with younger adults
(21–37 years).68 Gut bacterial populations in elderly individu-
als are characterized by reduced bacterial diversity and a
decrease in beneficial microorganisms, linked to diet and life-
style.69,70
Further investigation into the effect of ageing on the micro-
biome and the role of the skin microbiome in AD pathogene-
sis is needed. Increased AD severity in the elderly may be
related to greater S. aureus colonization and infection because
of its role in AD development in the general population.
Environmental factors
Patients with AD are often hyperresponsive to environmental
irritants and more likely to develop other atopic condi-
tions.36,71 These patients often have high IgE levels specific to
common allergens.36 Certain foods such as milk, eggs and
wheat, and environmental allergens including animal dander,
© 2019 British Association of Dermatologists
Atopic dermatitis in the elderly, S. Williamson et al. 51
grasses and pollens can trigger AD. Food allergy plays a more
significant role in inducing AD symptoms in children than in
older patients, and adult and elderly patients with AD who
have moderate-to-severe disease tend to have greater sensitiza-
tion to food allergens compared with patients who have
milder AD.9 Elderly patients with AD are most sensitive to
dust mites and pollens, measured by increased serum IgE
levels specific to these allergens,9 and less allergic to foods,
animal dander and fungi.7 However, elderly patients with
more severe AD, in particular, display allergic sensitivity to
various allergens.9 Elderly patients most often have hypersensi-
tivity to fragrance mixes including balsam of Peru and metals
including nickel and cobalt.72–74
In summary, this pathophysiology section reports evidence
of common changes observed with ageing that may constitute
risk factors for triggering or worsening AD in the elderly pop-
ulation (summary in Fig. 1 and Table 1). While general phys-
iological alterations with ageing overlap with key features of
AD, a research gap exists regarding specific ageing-related
changes in AD disease development. It must be noted that the
majority of people diagnosed with AD experience disease reso-
lution before adulthood, and most infants with AD have com-
plete remission before age 2 years.5 Why certain individuals
outgrow AD while others develop more persistent endotypes
or late-onset AD remains to be understood. It is tempting to
propose the hypothesis that in order to reach a level of disease
state in predisposed patients, a certain ‘threshold’ of skin bar-
rier impairment and/or immunological abnormalities needs to
be achieved. While some of these defects that present early in
life might be compensated for in childhood, others might be
worsened later in life as part of the physiological ageing pro-
cess. Future studies are needed to provide greater clarity
regarding the factors contributing to both AD progression and
resolution.
Diagnosis and management
There is a lack of specific guidelines available for physicians to
distinguish AD from other pruritic skin conditions in the
elderly. Compared with other age groups, the elderly tend to
have more comorbidities and medications that can cause pru-
ritus and xerosis, rendering the diagnosis of AD more diffi-
cult.7 Currently, older patients are diagnosed with AD after at
least 6 months7 of symptom assessment and exclusion of other
conditions,7 including cutaneous T-cell lymphoma,75 allergic
contact dermatitis,5 drug reactions,7 and chronic idiopathic or
secondary erythroderma.7 Bieber et al. recently stated that AD
in the elderly has not been well characterized as a specific
phenotype of AD and that clearer criteria for diagnosis are
necessary.5
There is a lack of information regarding AD treatment
specifically for the elderly. Tanei and Hasewaga stated that
elderly patients should currently be treated according to the
standardized guidelines for general AD treatment.7 From a
practical point of view, the treatment of elderly patients with
AD is complicated by several age-dependent factors and
British Journal of Dermatology (2020) 182, pp47–54
52 Atopic dermatitis in the elderly, S. Williamson et al.
comorbidities that the physician must consider. For example,
high blood pressure and reduced kidney function might limit
the use of ciclosporin, whereas diabetes, high blood pressure
and osteoporosis raise concerns for initiating systemic steroid
treatment. An increased propensity for infection in the elderly
can restrict the use of systemic immunosuppressant medica-
tions. Thinning of the skin with diffuse photoageing might
even limit the use of topical steroids. Decreased physical
mobility of elderly patients may further reduce the ability to
moisturize the skin properly and apply topical treatments.
This is an exciting time for developments in the treatment
of AD as the first biological medication (dupilumab) has been
approved by the U.S. Food and Drug Administration, and
more biological and small molecule medications are in the
pipeline.76–78 However, adult clinical trials traditionally enrol
only patients aged 18–65 years, thus excluding a large propor-
tion of the elderly. Further studies and clearer guidelines for
treating AD in the elderly need to be developed. Elderly
patients with AD rarely achieve complete disease remission,
and many affected patients eventually die with the condition.7
Conclusions
Studies estimate that 2–3% of the elderly population is
affected by AD, yet despite its prevalence, there is a knowl-
edge gap hindering diagnosis and treatment. Many prior AD
studies have not isolated this population from other age
groups, though doing so reveals important differences in dis-
ease manifestation. Factors rendering the elderly susceptible to
AD include innate physiological changes of ageing, notably
decline in skin barrier function, dysregulation of innate
immune cells, and skewing of adaptive immunity to a Th2
response. As the number of elderly people increases world-
wide, the disease burden of this relatively undescribed condi-
tion can be anticipated to increase in both personal and
societal cost. The pruritus, painful broken skin, and infections
associated with AD contribute to a decline in quality of life
and an increased financial and public health burden. More
knowledge about elderly AD is needed to establish firm diag-
nostic and treatment methodologies. Prompt and adequate care
that achieves remission could ensure a robust quality of life
and allay the higher healthcare costs associated with hospital-
ization for severe AD. Detailed studies of the integumentary
and immune systems of elderly patients with AD are necessary
so that treatment regimens can be tailored for these patients
and their care can be standardized more effectively.
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